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Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Atherosclerosis IV: Nursing Management01:23

Atherosclerosis IV: Nursing Management

Nursing management for a patient with arteriosclerosis involves a comprehensive approach focusing on lifestyle modification, disease monitoring, education, and symptomatic care. Here is an overview of effective nursing strategies:Assessment and Monitoring: Initial and ongoing assessments are crucial. Nurses must document the patient's medical history, including any hypertension, diabetes, hyperlipidemia, and other cardiovascular diseases. Assessments also cover family history and lifestyle...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...

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Related Experiment Video

Updated: May 12, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

The UPR in atherosclerosis.

Alex X Zhou1, Ira Tabas

  • 1Department of Medicine, Columbia University, New York, NY, USA. alex.zhou@wlab.gu.se

Seminars in Immunopathology
|April 5, 2013
PubMed
Summary
This summary is machine-generated.

Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) play dual roles in atherosclerosis, promoting survival early on but causing cell death and plaque instability later. Targeting UPR offers potential therapeutic strategies.

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Published on: October 3, 2017

Area of Science:

  • Cardiovascular Biology
  • Cellular Stress Response
  • Atherosclerosis Pathogenesis

Background:

  • Endoplasmic reticulum (ER) stress, triggered by systemic factors and local arterial wall stressors, affects endothelial cells (ECs), smooth muscle cells (SMCs), and macrophages.
  • The unfolded protein response (UPR), initiated by PERK, IRE1α, and ATF6 sensors, is a cellular mechanism to restore ER homeostasis.

Purpose of the Study:

  • To elucidate the temporal activation patterns and dual roles of UPR signaling pathways in different stages of atherosclerosis.
  • To investigate the implications of UPR-mediated cell death in plaque instability and clinical progression.
  • To explore the potential of UPR-targeting therapies for atherosclerosis prevention and regression.

Main Methods:

  • Analysis of UPR pathway activation (ATF6, IRE1α, PERK) in relation to cellular changes (ECs, SMCs, macrophages) and disease progression in atherosclerosis models.
  • Investigating the link between prolonged ER stress, enhanced UPR signaling, and UPR-mediated apoptosis in advanced lesions.
  • Examining the association of UPR signaling with inflammation and macrophage differentiation within atherosclerotic plaques.

Main Results:

  • ATF6 and IRE1α pathways are activated early in ECs, promoting chaperone expression.
  • PERK pathway activation occurs in SMCs and macrophages in early lesions, reducing protein load.
  • Prolonged ER stress and enhanced UPR signaling in advanced lesions promote apoptosis of SMCs and macrophages via PERK and IRE1α, contributing to plaque instability.

Conclusions:

  • UPR signaling exhibits stage-specific roles in atherosclerosis, initially promoting cell survival and later inducing apoptosis.
  • UPR-mediated cell death is linked to plaque instability and disease progression.
  • Targeting UPR pathways presents a promising therapeutic avenue for atherosclerosis, though further research is needed.